Background

Bilateral vocal fold (vocal cord) immobility (BVFI) is a broad term that refers to all forms of reduced or absent movement of the vocal folds. Bilateral vocal fold (cord) paralysis (BVFP) refers to the neurologic causes of bilateral vocal fold immobility (BVFI) and specifically refers to the reduced or absent function of the vagus nerve or its distal branch, the recurrent laryngeal nerve (RLN). Vocal fold immobility may also result from mechanical derangement of the laryngeal structures, such as the cricoarytenoid (CA) joint.

Direct laryngoscopic view of the larynx in a patient who with bilateral vocal fold immobility (BVFI) is shown. Palpation of the arytenoids revealed cricoarytenoid (CA) joint ankylosis. Close inspection of the interarytenoid space demonstrated interarytenoid scar. This condition is posterior glottic stenosis (PGS).

Although a small number of conditions account for most cases of vocal cord immobility, this article presents a comprehensive differential diagnosis, followed by the clinical presentations, diagnostic workup, and treatment options. The goal of the article is to provide the clinician with a basic understanding of the rare entity of bilateral vocal fold immobility (BVFI).
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History of the Procedure

The history of the procedures used to treat vocal cord immobility begins in 1855 with Garcia's work on mirror laryngoscopy. In the 1860s, Turk and Knight first described vocal cord paralysis. In 1922, Chevalier Jackson performed the first surgical procedure for bilateral vocal fold immobility (BVFP) when he endoscopically resected a vocal cord. He provided an airway at the expense of voice and airway protection. This dilemma continues to plague present surgeons. Since 1922, pioneers in laryngology have described arytenoidectomy, described vocal cord lateralization, and introduced the use of laser.

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Etiology

According to Benninger's findings in a series of 117 cases BVFI can be attributed to the following causes: surgical trauma (44%), malignancies (17%), endotracheal intubation (15%), neurologic disease (12%), and idiopathic causes (12%).
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Causes of vocal fold fixation differ in adults and in children. In adults, these include mechanical causes, inflammatory processes (affecting the CA or larynx), malignancy, surgery, neurologic causes, radiation injury, metabolic causes, and toxins. Mechanical derangement of the posterior glottis may also be referred to as posterior glottic stenosis (PGS). Bogdasarian and Olson classified PGS into the following 4 grades:
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Toxins

Central neurologic abnormalities

Central neurologic abnormalities account for most cases of childhood bilateral vocal fold paralysis (BVFP). Arnold-Chiari deformity with meningomyelocele and hydrocephalus is the most common abnormality. Other CNS insults (eg, infarct, craniotomy, asphyxia) account for some cases, according to the findings in a study by Rosin et al.
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Idiopathic causes

Idiopathic causes are the second most common causes of childhood bilateral vocal fold paralysis (BVFP). Some researchers postulate that the etiology in some children with bilateral vocal fold paralysis (BVFI) is an imbalance between the adductors and abductors of the larynx that results in adducted vocal folds. With time, a balance is restored and symptoms abate as children mature. Although conjectural, this explanation fits with the clinical course of most children with bilateral vocal fold paralysis (BVFI) who spontaneously improve with time. Gacek hypothesized that fewer abductor fibers exist; therefore, injury to the nerve is more likely to cause abductor dysfunction.
[10] He also conjectured that, since abductor fibers are phylogenetically younger than adductor fibers, they may be more fragile.

Iatrogenic causes

Pathophysiology

Although a comprehensive discussion of each of the causes is beyond the scope of this article, some principles should be emphasized. With the first episode of bilateral vocal fold paralysis (BVFP), patients may have dysphonia because the vocal cords are too far apart. Over time, however, the vocal cords can move to a medial position, and the patient may have a good voice and cough despite stridor and bilateral vocal fold paralysis (BVFP). As the vocal cords migrate toward the midline, the voice (and cough) improves, while the airway worsens. Clinicians should not mistake a good voice and cough as signs of a functioning larynx, especially in a patient with stridor. Aspiration and dysphagia may or may not be present in patients with vocal cord paralysis.

In terms of the pathophysiology of CA fixation, inflammatory or fibrotic changes can paralyze or reduce the mobility of the joint. Various disorders can cause these changes.

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Presentation

History

The importance of a complete history cannot be overstated. The history should include the following:

For patients with bilateral vocal fold paralysis (BVFP) due to iatrogenic injury in which the recurrent laryngeal nerve (RLN) or vagus nerve is injured (neurapraxia) but not severed, permanent surgical treatment should be postponed for at least 9 months after injury to allow spontaneous recovery. Laryngeal electromyographic (EMG) monitoring can be helpful in obtaining an index of potential recovery. Obtaining a baseline EMG 30-40 days after injury and second EMG 1 month later can help in evaluating the recovery status of the vocal cords (Munin).
[12] On the basis of the surgeon's clinical judgment, tracheostomy for patients with quickly deteriorating airways should be initiated quickly.

For adult patients with bilateral vocal fold (cord) paralysis (BVFP), the literature supports use of an endoscopic approach, with either posterior cordectomy or limited arytenoidectomy as the initial procedure of choice. Suture lateralization may play an adjunctive role. All of these are static permanent procedures; therefore, they should be undertaken only after spontaneous improvement has failed to occur or if EMG findings suggest permanent injury.

For patients with bilateral vocal fold immobility (BVFI) caused by PGS, serial endoscopic approaches with scar lysis or microflap trapdoor reconstruction of the interarytenoid (IA) region can be attempted before the static procedures are used.

Airway obstruction refractory to the above measures is particularly vexing. Treatment options include laryngofissure with arytenoidectomy, IA reconstruction, posterior cricoidotomy with stent placement, or posterior cricoidotomy with grafting. The literature is less clear concerning the indications for each of these approaches than those of other procedures.

Children

Surgical intervention is indicated when respiratory effects are significant. Cordopexy or arytenoidopexy, along with partial or complete arytenoidectomy, can help solve the airway problem during the ensuing months or years as one waits for possible recovery of the contralateral cord. Children with bilateral vocal fold paralysis (BVFP) require tracheostomy only when the airway fails to improve with other measures. Findings of a literature review suggest that the airway can be managed expectantly, without a tracheostomy. Endoscopic management plays a limited role in children and is useful only for mild fixed stenosis and for revisional procedures in children who have undergone open procedures.

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Relevant Anatomy

A review of vagus nerve and RLN anatomy is necessary to understand potential injuries that can cause vocal cord paralysis. The vagus nerve originates in the nucleus ambiguus of the medulla oblongata. At that point, it is composed of cells that receive neural input from the Broca area via decussating corticobulbar tracts; thus it provides input to both the right and left nuclei. Neural input from the cerebellum and extrapyramidal centers, as well as from visceral afferents, provides proprioceptive input that modulates the motor function of the vagus nerve at this site.

The motor fibers or visceral efferents that affect the larynx and pharynx occupy 2 specific sites within the nucleus ambiguus. One site becomes the superior laryngeal nerve (SLN); the other, the RLN. The vagus nerve leaves the medulla and enters the jugular foramen, along with the accessory nerve and jugular vein. Within the jugular foramen, the vagus nerve widens to form the superior ganglion, where the cell bodies of the sensory component of the nerve reside (somatic sensory). They provide sensation to the ear canal skin (Arnold nerve). As the vagus nerve exits the jugular foramen, it widens again to form the nodose ganglion, in which nerve cell bodies containing the sensory or visceral afferents from the larynx and pharynx reside.

Immediately distal to the nodose ganglion, the SLN exits the vagus nerve and courses along the carotid artery to the larynx, where it enters the larynx through the thyrohyoid membrane, dividing into internal and external branches. The internal branch provides sensory function (visceral afferent), and the external branch provides motor function to the cricothyroid muscle (visceral efferent). The vagus nerve then descends in the neck immediately lateral to the carotid artery.

The right RLN fibers exit from the vagus nerve as the nerve crosses anteriorly over the subclavian artery. The RLN loops posteriorly around the subclavian artery to enter the larynx through the Killian-Jamieson area or superior to the fibers of the cricopharyngeal muscle entering the larynx at the cricothyroid space.

The left RLN divides much further in the mediastinum, exiting the vagus nerve as it crosses anterior to the aorta and lateral to the ligamentum arteriosum (ie, remnant of the patent ductus arteriosum between the aorta and the pulmonary vein). It then extends superiorly to enter the larynx opposite the right RLN. The RLN branches into the posterior sensory branch and the motor anterior branch to the posterior cricoarytenoid (PCA), IA, lateral cricoarytenoid (LCA), and thyroarytenoid (TA) muscles. The IA muscle is the only motor branch that receives bilateral innervation, which allows some movement of both vocal folds when one RLN is nonfunctional.

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Contraindications

In adults, any definitive procedure to address vocal cord paralysis, whether unilateral or bilateral, must not be undertaken while a possibility for recovery exists. Recovery can occur as long as 12 months after injury. Every attempt must be made to determine if function is likely to return. This determination should include video direct laryngoscopy, during which the vocal fold can be palpated to assess mobility and bronchoscopy. In addition, laryngeal EMG can be used to evaluate normal action potentials (normal nerve), the absence of potentials (nonfunctioning nerve), defibrillating potentials (worsening nerve), or polyphasic potentials (regenerating nerve). The 12-month wait for return of function can be shortened by obtaining 2 laryngeal EMGs several months apart and by looking for evidence of improved function or stabilized function.
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As many as 70% of children with bilateral vocal fold (cord) paralysis (BVFP) require a tracheostomy. However, spontaneous recovery occurs in half of the patients, sometimes in those as old as11 years. If the condition spontaneously resolves, it typically does so 24-36 months after diagnosis. Therefore, destructive static procedures should be delayed for approximately 3 years because of this potential for recovery. Delaying surgery in children with bilateral vocal fold (cord) immobility (BVFI) caused by PGS is not beneficial; consequently, bilateral vocal fold immobility (BVFI) must be diagnosed correctly in these children to prevent restriction from surgical repair.

Direct laryngoscopic view of the larynx in a patient who with bilateral vocal fold immobility (BVFI) is shown. Palpation of the arytenoids revealed cricoarytenoid (CA) joint ankylosis. Close inspection of the interarytenoid space demonstrated interarytenoid scar. This condition is posterior glottic stenosis (PGS).

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cerescan;RxRevu;Cliexa;Preacute Population Health Management;The Physicians Edge<br/>Received income in an amount equal to or greater than $250 from: The Physicians Edge, Cliexa<br/> Received stock from RxRevu; Received ownership interest from Cerescan for consulting; for: Rxblockchain;Bridge Health.

Additional Contributors

Clark A Rosen, MD Director, University of Pittsburgh Voice Center; Professor, Department of Otolaryngology and Communication Science and Disorders, University of Pittsburgh School of Medicine

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Merz North America Inc<br/>Received consulting fee from Merz North America Inc for consulting; Received consulting fee from Merz North America Inc for speaking and teaching.

Acknowledgements

Arturo Avila Chavez, MD Assistant Professor, Department of Otolaryngology and Head and Neck Surgery, Instituto Nacional De Enfermedades Respiratorias of Mexico City